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Today's software systems communicate over the Internet using standard protocols that have been heavily scrutinized, providing some assurance of resistance to malicious attacks and general robustness. However, the software that implements those protocols may still contain mistakes, and an incorrect implementation could lead to vulnerabilities even in the most well-understood protocol. The goal of this work is to close this gap by introducing a new technique for checking that a C implementation of a protocol matches its description in an RFC or similar standards document. We present a static (compile-time) source code analysis tool called Pistachio that checks C code against a rule-based specification of its behavior. Rules describe what should happen during each round of communication, and can be used to enforce constraints on ordering of operations and on data values. Our analysis is not guaranteed sound due to some heuristic approximations it makes, but has a low false negative rate in practice when compared to known bug reports. We have applied Pistachio to two different implementations of SSH2 and an implementation of RCP. Pistachio discovered a multitude of bugs, including security vulnerabilities, that we confirmed by hand and checked against each project's bug databases. (C) 2007 Elsevier Inc. All rights reserved.

Signal transducer and activator of transcription (STAT) comprises a family of universal transcription factors that help cells sense and respond to environmental signals. STAT5 refers to two highly related proteins, STAT5A and STAT5B, with critical function: their complete deficiency is lethal in mice; in humans, STAT5B deficiency alone leads to endocrine and immunological problems, while STAT5A deficiency has not been reported. STAT5A and STAT5B show peptide sequence similarities greater than 90%, but subtle structural differences suggest possible non-redundant roles in gene regulation. However, these roles remain unclear in humans. We applied chromatin immunoprecipitation followed by DNA sequencing using human CD4(+) T cells to detect candidate genes regulated by STAT5A and/or STAT5B, and quantitative-PCR in STAT5A or STAT5B knock-down (KD) human CD4(+) T cells to validate the findings. Our data show STAT5A and STAT5B play redundant roles in cell proliferation and apoptosis via SGK1 interaction. Interestingly, we found a novel, unique role for STAT5A in binding to genes involved in neural development and function (NDRG1, DNAJC6, and SSH2), while STAT5B appears to play a distinct role in T cell development and function via DOCK8, SNX9, FOXP3 and IL2RA binding. Our results also suggest that one or more co-activators for STAT5A and/or STAT5B may play important roles in establishing different binding abilities and gene regulation behaviors. The new identification of these genes regulated by STAT5A and/or STAT5B has major implications for understanding the pathophysiology of cancer progression, neural disorders, and immune abnormalities.